Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Baylor Genetics | RCV000006389 | SCV004200038 | likely pathogenic | Mitochondrial complex 1 deficiency, nuclear type 9 | 2023-04-11 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV003555940 | SCV004292802 | likely pathogenic | not provided | 2023-06-15 | criteria provided, single submitter | clinical testing | In summary, the currently available evidence indicates that the variant is pathogenic, but additional data are needed to prove that conclusively. Therefore, this variant has been classified as Likely Pathogenic. This variant disrupts the p.Cys115 amino acid residue in NDUFS6. Other variant(s) that disrupt this residue have been determined to be pathogenic (PMID: 28429146, 30948790). This suggests that this residue is clinically significant, and that variants that disrupt this residue are likely to be disease-causing. An algorithm developed to predict the effect of missense changes on protein structure and function (PolyPhen-2) suggests that this variant is likely to be disruptive. ClinVar contains an entry for this variant (Variation ID: 6018). This missense change has been observed in individuals with mitochondrial complex I deficiency (PMID: 19259137). This variant is present in population databases (rs267606913, gnomAD 0.01%). This sequence change replaces cysteine, which is neutral and slightly polar, with tyrosine, which is neutral and polar, at codon 115 of the NDUFS6 protein (p.Cys115Tyr). |
OMIM | RCV000006389 | SCV000026571 | pathogenic | Mitochondrial complex 1 deficiency, nuclear type 9 | 2009-09-01 | no assertion criteria provided | literature only |